Neurotoxicology
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A major challenge for physicians is to identify patients with acute carbon monoxide (CO) poisoning who are likely to develop delayed neuropsychiatric sequelae (DNS). DNS is defined as neuropsychological sequelae that develops after 2-40 days of lucid interval after CO intoxication. Currently, there is no consensus on factors that predict the prognosis of CO poisoning. Thus, the purpose of this study was to identify factors predicting the development of DNS using a Cox regression model. ⋯ In acute CO poisoning, an initial GCS score ≤ 9 and serum CK level > 175.5 U/L are significant predictors of DNS development.
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General anesthesia induces changes in dendritic spine number and synaptic transmission in developing mice. These changes are rather disturbing, as similar changes are seen in animal models of neurodevelopmental disorders. We previously suggested that mTor-dependent upregulation of mitochondrial function may be involved in such changes. ⋯ We next assessed whether the mitochondrial unfolded protein response (UPRmt) acted as a link between anesthetic exposure and mitochondrial function. Expression of UPRmt proteins, which help maintain protein-folding homeostasis and increase mitochondrial function, was increased 6 h after sevoflurane exposure. Our results show that a single, brief sevoflurane exposure induces age-dependent changes in mitochondrial function that constitute an important mechanism for the increase in excitatory synaptic transmission in late postnatal mice, and also suggest mitochondria and UPRmt as potential targets for preventing anesthesia toxicity.